Three hormonal systems - kallikrein-kinin, renin-angiotensin and prostaglandin - having major representation within the kidney will be examined as they interact through several important enzymes, chiefly prostaglandin related, that can affect their level of activity. Vasoactive polypeptides - kinins, angiotensins, and vasopressin -not only affect the activity of acylhydrolases such as phospholipase Alpha-2, but also that of PGE-9-ketoreductase; the latter determines the ratio of PGE2/PGF2 alpha intrarenally. The effect of other hormones and changes in salt intake on these interactions will be studied. The use of an angiotensin converting enzyme inhibitor may facilitate kinin-prostacyclin interactions in the renal vasculature; thus, the abundance of kininase II in this tissue usually blunts or prevents this interaction. Interaction of angiotensins I and II with prostacyclin metabolizing enzymes in the renal vasculature will be sought, particularly possible facilitation by a converting enzyme inhibitor of angiotensin I induction of prostacyclin synthetase. The mechanism of action of several classes of antihypertensive agents will be examined as they might influence prostaglandin metabolizing enzymes and modify the effects of vasoactive hormones on prostaglandin releasing mechanisms. Interactions of these hormonal systems will be explored in experimental hypertension and in normotensive and hypertensive pregnant rats. Prostacyclin metabolism in liver, kidney and vascular tissue will be studied, using GC-MS, as recent results suggest that metabolites having greater stability than the parent compound and a similar potency and range of activity can be generated in these organs. Thus, metabolizing enzymes not only determine prostaglandin degradation but may transform an inactive to an active substance, e.g., 6-keto-PGF1-alpha to 6-keto-PGE1.